NOVEL COMPOUNDS AND THEIR USE AS PHOTODYNAMIC AGENTS The invention relates to compounds of formula (I) and derivatives thereof. These compounds act as photosensitizing agents, that upon photon absorption generates cytotoxic reactive oxygen species. The invention also relates to pharmaceutical compositions comprising these compounds and to the use of these compounds as a DNA damaging agent and in the treatment of various forms of cancer, skin conditions, and ophthalmology conditions. BACKGROUND Exosomes are nanometre scale vesicles involved in inter-cellular signalling. When present inside the cell, the exosomes are localised inside multivesicular bodies (MVBs). At that time, they are commonly referred to as intraluminal vesicles (ILVs). Upon fusion of the MVB with the cell membrane, the intraluminal vesicles are released into the extracellular space, at which point they are referred to as exosomes (Grant, B.D. et al. Nat Rev Mol Cell Biol 10, 597-608 (2009) and Zhang, Y. et al. Cell Biosci 9, 19 (2019)). Bioactive molecules, such as DNA, RNA, and proteins, carried inside the exosome, are then transported from the inside of the cell to the outside of the cell. They are also involved in key biological processes including cell to cell communication (Balaj, L. et al. Nat Commun 2, 180 (2011); Thakur, B.K. et al. Cell Res 24, 766-9 (2014); Mateescu, B. et al. J Extracell Vesicles 6, 1286095 (2017); Li, I., et al. Mol Cancer 18, 32 (2019)). Exosome secretion by cancer cells is higher compared to their healthy counterpart, and tumour cell-derived exosomes are highly enriched in genomic DNA with up to a 20-fold enrichment compared to those derived by healthy cells (Yokoi, A. et al. Sci Adv 5, eaax8849 (2019)). Consequently, DNA-rich, tumour-derived exosomes are important biomarkers for cancer detection and targeting. Guanine (G)-rich DNA sequences can fold into non-canonical four-stranded structures, so-called G-quadruplexes (G4s). The position of G4 structures is predicted not to be randomly spread in the nuclear genome, but enriched at certain areas i.e., at promoters, at ribosomal DNA, and at telomeres (Varshney, D et al. Nat Rev Mol Cell Biol 21, 459-474 (2020)). Recent studies involving the G4 specific antibody (BG4) (Biffi, G. et al. Nat Chem 5, 182-6 (2013) and Biffi, G. et al. PLoS One 9, e102711 (2014)), live-cell fluorescent probes (Liu, L.Y. et al. Angew Chem Int Ed Engl 59, 9719-9726 (2020); Deiana, M. et al. ACS Chem Biol 16, 1365-1376 (2021) and Di Antonio, M. et al. Nat Chem 12, 832-837 (2020)) , and chromatin immunoprecipitation followed by high throughput sequencing (ChIP-Seq) (Hänsel-Hertsch, R. et al. Nat Genet 48, 1267-72 (2016); Hänsel-Hertsch, R. et al. Nat Protoc 13, 551-564 (2018); De, S. et al. Nat Struct Mol Biol 18, 950- 5 (2011) and Hänsel-Hertsch, R. et al. Nat Genet 52, 878-883 (2020)), revealed increased levels of G4 structures in cancer cells compared to normal cells. Moreover, G-rich sequences are sensitive to reactive oxygen species (ROS) (Fleming, A.M. & Burrows, C.J. et al. J Am Chem Soc 142, 1115-1136 (2020)). When exposed to ROS, they form oxidatively modified G base lesions, commonly the oxo-7,8-dihydro-2ʹ-deoxyguanosine (8-oxoG) mutation. This sensitivity to oxidative stress can be applied in cancer therapeutics to induce cancer cell death, especially as many cancer cells have impaired DNA damage response (DDR) machinery. Light-activated anticancer strategies, including photodynamic therapy (PDT), have been established as safe, non-surgical methods for treating numerous cancer types. PDT involves the administration of a photosensitizing (PS) agent that upon photon absorption promotes the generation of cytotoxic reactive oxygen species (ROS). The primary selectivity of PDT is due to the control of the illumination of particular regions with high spatiotemporal precision. In the past years, a number of organelle-selective PS agents targeting the nuclei, mitochondria and lysosomes have been reported and their phototherapeutic properties deeply investigated, for example by Wang et. al. (ACS Appl Mater Interfaces 13, 19543-19571 (2021)). However, the majority of these PS agents show relatively low triplet quantum yields and phototoxicity index (the ratio of the IC 50 values in the dark to those obtained upon light irradiation). Moreover, the incorporation of heavy atoms to enhance intersystem crossing (ISC), rises concerns about systemic toxicity, costs, and safety. Even though PDT is well known in the art as a treatment method for cancer, there is still a need for photosensitizing agents with improved selectivity for the relevant regions of the cell. In addition, the PS agents need to have a low systemic toxicity and be effective in low doses. BRIEF DESCRIPTION OF THE DRAWINGS Fig.1 shows the quantification of nuclear ROS signal in non-irradiated and irradiated DBI-treated HeLa cells. Fig.2 shows the cytotoxic effects of 2-(pentan-3-yl)-1H-benzo[7,8]thioxantheno[2,1,9- def]isoquinoline-1,3(2H)-dione (DBI) on a) HeLa cells and b) MCF-7 cells. Fig.3 shows the cytotoxic effects of 2-(pentan-3-yl)benzo[lmn]naphtho[2,1- c][2,8]phenanthroline-1,3(2H,6H)-dione on HeLa cells a) without light, and b) with light. Fig 4 shows the cytotoxic effects of 2-(pentan-3-yl)-1H-benzo[7,8]xantheno[2,1,9- def]isoquinoline-1,3(2H)-dione on HeLa cells a) without light, and b) with light. Fig.5 shows the cytotoxic effects of DBI on tumor organoids. Fig.6 shows growth of yeast cells in liquid media containing a reference or DBI after light treatment. DETAILED DESCRIPTION OF THE INVENTION The present invention discloses heavy-metal free photosensitizers that feature a twisted π- conjugated system providing enhanced intersystem crossing capabilities and consequential singlet oxygen ( ¹ O2) generation efficiency, designed to overcome the limitations outlined in the background. In particular, the disclosed compounds show high phototherapeutic efficacy at low nanomolar concentrations against monolayer cancer cells and 3D tumour organoids. The high cytotoxicity is demonstrated by in vivo experiments on zebrafish embryos. The compounds of the invention are shown to be accumulated in ILVs/exosomes as well as its subcellular G4 structures. The photoinduced generation of ¹ O ₂ reveals a close connection between DNA damage, G4 structures, and replicative stress that ultimately lead to cell death. The dual targeting of cancer mediators/markers ILVs/exosomes and G4s renders the present compounds very suitable for broad biomedical applications, for example treatment of cancer, various skin conditions, bacterial infections, and ophthalmology conditions. Moreover, the present compounds show a high phototherapeutic efficacy even in systems with reduced oxygen supply. In a first aspect, the invention relates to a compound of formula (I) or a pharmaceutically acceptable salt thereof, wherein R ¹ is selected from a group consisting of C _1-20 alkyl, C _3-6 cycloalkyl, COOH, C _1-20 COOH, COOC _1-20 alkyl, COC _1-20 alkyl, CONHC _1-20 alkyl, C _1-20 alkyl sulphonate, C _1-20 alkyl phosphonate, C _6-20 aryl, C _4-20 heteroaryl, C _1-4 alkyloxy C _1-4 alkyl sulphonate, methyl (C _1-4 alkyloxy C _1-4 alkyl sulphonate) ₂ , C _1-4 alkyl terminally substituted with a C _5-6 heterocyclyl with one or two heteroatoms being O, S or N, C _1-4 alkyl terminally substituted with N(C _1-4 alkyl)(C _1-4 alkyl), polyethylene glycol, an amino acid, zwitterionic (C1-4 alkyl)N ⁺ (C1-4 alkyl)2(C1-4 alkyl SO3-), (C1-4 alkyl)N ⁺ (C1-4 alkyl)2O-, cationic (C1-4 alkyl)N ⁺ (C _1-4 alkyl) ₃ , (C _1-4 alkyl)P ⁺ (C _1-4 alkyl) ₃ , (C _1-4 alkyl)P ⁺ (Ph) ₃ , and osamine; R ² , R ³ and R ⁴ are independently selected from the group consisting of hydrogen, halogen, NO2, CN, CF3, polyethylene glycol, C1-20 alkyl, C6-20 aryl, C4-20 heteroaryl, C1-20 alkyl sulphonate, and C1-20 alkyl phosphonate; X and Y are independently selected from O or SOm, where m=0-2; and A is selected from the group consisting of O, S, NR ⁵ , or Se, wherein R ⁵ is selected from the group consisting of H, C1-20 alkyl, COOH, COOC1-10 alkyl, COC1-20 alkyl, CONHC1-20 alkyl, C1-20 alkyl sulphonate, C1-20 alkyl phosphonate, C6-20 aryl, C4-20 heteroaryl, with the proviso that when X, Y, and A simultaneously are O, and R ² and R ³ are both H, then R ¹ is not any one of: Preferably, when R ² and R ³ are both H, and A, X and Y are simultaneously O, then R ¹ is not alkyl, cycloalkyl, aryl, alkoxy, or amino. As used herein, the term “C _1-20 alkyl” refers to a straight or branched alkyl group having from 1 to 20 carbon atoms. Examples of C1-20 alkyl include methyl, propyl, isopropyl, butyl, isobutyl, tert-butyl, octyl, dodecyl, heptadecyl and icosyl. As used herein, the term “C3-6 cycloalkyl” refers to a monocyclic saturated hydrocarbon ring having from 3 to 6 carbon atoms. Examples of C3-6 cycloalkyl include cyclopropyl, cyclobutyl, cyclopentyl and cyclohexyl. As used herein, the terms “COOC1-20 alkyl”, “COC1-20 alkyl”, and “CONHC1-20” refers to a straight or branched alkyl group being attached to the nitrogen atom of formula (I) via an ester, a ketone, or an amide, where the nitrogen atom of formula (I) is bound the carbonyl carbon in the respective moieties. As used herein, the terms “C1-20 alkyl sulphonate” and “C1-20 alkyl phosphonate” refers to a straight or branched alkyl group being attached to the nitrogen atom of formula (I) via a sulphonate or a phosphonate group. As used herein, the term “C _6-20 aryl” refers to an aryl group having 6-20 carbon atoms, having one or more aromatic rings. Examples of C6-20 aryl include phenyl, naphthyl, terpenyl, phenantryl, and antracyl. As used herein, the term “C _4-20 heteroaryl” refers to an aryl group having 4-20 carbon atoms, and wherein one or more atom is N, O or S, and having one or more aromatic rings. Examples of C _4-20 heteroaryl include pyridyl, triazyl, and azanaphthyl. In some embodiments, the invention relates to a compound of formula (I), wherein R ¹ is selected from a group consisting of C1-20 alkyl, C3-6 cycloalkyl, COOH, COOC1-20 alkyl, COC1-20 alkyl, CONHC _1-20 alkyl, C _1-20 alkyl sulphonate, C _1-20 alkyl phosphonate, C _6-20 aryl, C _4-20 heteroaryl, C _1-4 alkyloxy C _1-4 alkyl sulphonate, methyl (C _1-4 alkyloxy C _1-4 alkyl sulphonate) ₂ , C _1-4 alkyl terminally substituted with a C _5-6 heterocyclyl with one or two heteroatoms being O, S or N, C _1-4 alkyl terminally substituted with N(C _1-4 alkyl)(C _1-4 alkyl), polyethylene glycol, an amino acid, zwitterionic (C _1-4 alkyl)N ⁺ (C _1-4 alkyl) ₂ (C _1-4 alkyl SO ₃ -), cationic (C _1-4 alkyl)N ⁺ (C _1-4 alkyl) ₃ , (C _1-4 alkyl)P ⁺ (C1-4 alkyl)3, (C1-4 alkyl)P ⁺ (Ph)3, and osamine. In some embodiments, R ¹ is an amino acid selected from the group consisting of alanine, arginine, asparagine, aspartic acid, cysteine, glutamic acid, glutamine, glycine, histidine, hydroxyproline, isoleucine, leucine, lysine, methionine, phenylalanine, proline, serine, threonine, tryptophan, tyrosine, valine, and an amino acid according to formula (II), wherein R ⁶ is selected from a group consisting of C1-20 alkyl, COOC1-20 alkyl, COC1-20 alkyl, CONHC1-20 alkyl, C1-20 alkyl sulphonate, C1-20 alkyl phosphonate, C6-20 aryl, C4-20 heteroaryl, C1-4 alkyl terminally substituted with a C5-6 heterocyclyl with one or two heteroatoms being O, S or N, C1-4 alkyl terminally substituted with N(C _1-4 alkyl)(C _1-4 alkyl), polyethylene glycol, osamine; and wherein the N-terminal of the amino acid corresponds to the N-atom shown in formula (I). In one embodiment, R ¹ is C _1-20 alkyl, or any one of . In some embodiments, R ² and R ³ are independently selected from H, halogen, CF3, CN, and NO2. In some embodiments, R ² and R ³ are H. In some embodiments, R ⁴ is selected from H, halogen, CF ₃ , CN, and NO ₂ , preferably H. In some embodiments, R ⁵ is selected from the group consisting of C _1-20 alkyl, COOH, COOC _1-10 alkyl, COC _1-20 alkyl, CONHC _1-20 alkyl, C _1-20 alkyl sulphonate, C _1-20 alkyl phosphonate, C _6-20 aryl, C _4-20 heteroaryl. In some embodiments, A is S or NR ⁵ , wherein R ⁵ is defined as above. In some embodiments, A is S. In some embodiments, the compound is a 1H-benzo[7,8]thioxantheno[2,1,9-def]isoquinoline- 1,3(2H)-dione according to formula (I), substituted with R ¹ , R ² , R ³ , and R ⁴ as defined above. In a particular embodiment, the compound according to the present invention is selected from the group consisting of: 2-(pentan-3-yl)-1H-benzo[7,8]thioxantheno[2,1,9-def]isoquino line-1,3(2H)-dione, 2-(pentan-3-yl)benzo[lmn]naphtho[2,1-c][2,8]phenanthroline-1 ,3(2H,6H)-dione, 2-(pentan-3-yl)-1H-benzo[7,8]xantheno[2,1,9-def]isoquinoline -1,3(2H)-dione, 3-(1,3-dioxo-1H-benzo[7,8]thioxantheno[2,1,9-def]isoquinolin -2(3H)-yl)-N,N,N-trimethylpropan- 1-aminium, 3-(1,3-dioxo-1H-benzo[7,8]thioxantheno[2,1,9-def]isoquinolin -2(3H)-yl)-N,N-dimethylpropan-1- amine oxide, 3-(1,3-dioxo-1H-benzo[7,8]thioxantheno[2,1,9-def]isoquinolin -2(3H)-yl)propanoic acid, and 2-(3-(dimethylamino)propyl)-1H-benzo[7,8]thioxantheno[2,1,9- def]isoquinoline-1,3(2H)-dione. In a preferred embodiment, the compound of formula (I) is 2-(pentan-3-yl)-1H- benzo[7,8]thioxantheno[2,1,9-def]isoquinoline-1,3(2H)-dione (DBI) . The designed photosensitiser (PS) of the present invention is capable of enhanced intersystem crossing (ISC) from the excited singlet state to a long-lived triplet state and provides a close-to- unit singlet oxygen quantum yield, while remaining luminescent enough for in-situ detection and monitoring. Moreover, the compounds of the present invention target two cancer-specific mediators/markers in cells: - the DNA-rich tumor-derived ILVs/exosomes that are well-known cancer biomarkers; and - non-canonical DNA G4 structures which are promising targets for cancer therapy. Different functional groups can be used to target different areas in the cell. For example, ammonium and pyridinium are quite efficient in targeting the nucleus, while phosphonium are associated to mitochondrial targeting. The high phototoxic damage of the compounds of the present invention towards cancer cells is likely attributed to the accumulation in the ILVs and the binding to G4 structures. Additionally, phototoxicity toward 2D cancer cell models is high while remaining non-toxic under dark conditions. This is demonstrated by the biological studies presented below. The observed phototoxicity of the compounds can be linked to the interplay between guanine oxidation, double stranded DNA breaks, and G4 formation, ultimately leading to cell death. In another aspect, the invention relates to a pharmaceutical composition comprising a therapeutically effective amount of a compound according to formula (I), or a pharmaceutically acceptable salt thereof wherein R ¹ is selected from a group consisting of C1-20 alkyl, C3-6 cycloalkyl, COOH, C1-20 COOH, COOC1-20 alkyl, COC1-20 alkyl, CONHC1-20 alkyl, C1-20 alkyl sulphonate, C1-20 alkyl phosphonate, C6-20 aryl, C4-20 heteroaryl, C _1-4 alkyloxy C _1-4 alkyl sulphonate, methyl (C _1-4 alkyloxy C _1-4 alkyl sulphonate) ₂ , C _1-4 alkyl terminally substituted with a C _5-6 heterocyclyl with one or two heteroatoms being O, S or N, C _1-4 alkyl terminally substituted with N(C _1-4 alkyl)(C _1-4 alkyl), polyethylene glycol, an amino acid, zwitterionic (C _1-4 alkyl)N ⁺ (C _1-4 alkyl) ₂ (C _1-4 alkyl SO ₃ -), (C _1-4 alkyl)N ⁺ (C _1-4 alkyl) ₂ O-, cationic (C _1-4 alkyl)N ⁺ (C _1-4 alkyl) ₃ , (C _1-4 alkyl)P ⁺ (C _1-4 alkyl) ₃ , (C _1-4 alkyl)P ⁺ (Ph) ₃ , and osamine; R ² , R ³ and R ⁴ are independently selected from the group consisting of hydrogen, halogen, NO2, CN, CF ₃ , polyethylene glycol, C _1-20 alkyl, C _6-20 aryl, C _4-20 heteroaryl, C _1-20 alkyl sulphonate, and C _1-20 alkyl phosphonate; X and Y are independently selected from O or SOm, where m=0-2; and A is selected from the group consisting of O, S, NR ⁵ , or Se, wherein R ⁵ is selected from the group consisting of H, C1-20 alkyl, COOH, COOC1-10 alkyl, COC1-20 alkyl, CONHC1-20 alkyl, C1-20 alkyl sulphonate, C1-20 alkyl phosphonate, C6-20 aryl, C4-20 heteroaryl; and one or more pharmaceutically acceptable excipients, carriers, or diluents. In general, such pharmaceutical compositions may be prepared in a conventional manner using conventional excipients, carriers, and diluents. In some embodiments R ¹ , R ² , R ³ , R ⁴ , R ⁵ , X, Y and A are as defined in any of the embodiments above. The invention also relates to the use of the pharmaceutical composition according to the invention as a medicament. The pharmaceutical composition may be in a form that is suitable for oral administration, for parenteral injection (including intravenous, subcutaneous, intramuscular, and intravascular injection), for topical administration or for rectal administration. In a preferred embodiment, the pharmaceutical composition is in a form that is suitable for intravenous or topical administration. The dosage required for the therapeutic or prophylactic treatment will depend on the route of administration, the severity of the disease, the age and weight of the patient and other factors normally considered by the attending physician, when determining the appropriate regimen and dosage level for a particular patient. In another aspect, the invention relates to a compound of formula (I) or a pharmaceutically acceptable salt thereof,

wherein R ¹ is selected from a group consisting of C _1-20 alkyl, C _3-6 cycloalkyl, COOH, C _1-20 COOH, COOC _1-20 alkyl, COC _1-20 alkyl, CONHC _1-20 alkyl, C _1-20 alkyl sulphonate, C _1-20 alkyl phosphonate, C _6-20 aryl, C _4-20 heteroaryl, C _1-4 alkyloxy C _1-4 alkyl sulphonate, methyl (C _1-4 alkyloxy C _1-4 alkyl sulphonate) ₂ , C _1-4 alkyl terminally substituted with a C _5-6 heterocyclyl with one or two heteroatoms being O, S or N, C1-4 alkyl terminally substituted with N(C1-4 alkyl)(C1-4 alkyl), polyethylene glycol, an amino acid, zwitterionic (C1-4 alkyl)N ⁺ (C1-4 alkyl)2(C1-4 alkyl SO3-), (C1-4 alkyl)N ⁺ (C1-4 alkyl)2O-, cationic (C1-4 alkyl)N ⁺ (C1-4 alkyl)3, (C1-4 alkyl)P ⁺ (C1-4 alkyl)3, (C1-4 alkyl)P ⁺ (Ph)3, and osamine; R ² , R ³ and R ⁴ are independently selected from the group consisting of hydrogen, halogen, NO2, CN, CF3, polyethylene glycol, C1-20 alkyl, C6-20 aryl, C4-20 heteroaryl, C1-20 alkyl sulphonate, and C1-20 alkyl phosphonate; X and Y are independently selected from O or SOm, where m=0-2; and A is selected from the group consisting of O, S, NR ⁵ , or Se, wherein R ⁵ is selected from the group consisting of H, C1-20 alkyl, COOH, COOC1-10 alkyl, COC1-20 alkyl, CONHC1-20 alkyl, C1-20 alkyl sulphonate, C _1-20 alkyl phosphonate, C _6-20 aryl, C _4-20 heteroaryl, for use as a medicament. In some embodiments R ¹ , R ² , R ³ , R ⁴ , R ⁵ , X, Y and A are as defined in any of the embodiments above. In another aspect, the invention relates to a compound of formula (I) for use as a DNA damaging agent. The DNA damage can be in the form of oxidative base lesions such as 7,8-dihydro-8- oxoguanine or DNA strand breaks. In another aspect, the invention relates to a compound of formula (I) for use as G-quadruplex inducing agent. In another aspect, the invention relates to a compound of formula (I) for use as a marker for intraluminal vesicles or exosomes. Exosomes can be purified from biofluids, and using compounds of formula (I) as markers enables DNA damage assessment in a blood sample with fluorescence microscopy. Thereby the use of antibodies in immunofluorescence becomes redundant. Compounds of formula (I) can be used as a biomarker to monitor the treatment efficiency of PDT. In another aspect, the invention relates to a compound of formula (I) used for producing singlet oxygen. In another aspect, the invention relates to a compound of formula (I), wherein R ¹ is selected from a group consisting of C1-20 alkyl, C3-6 cycloalkyl, COOH, C1-20 COOH, COOC1-20 alkyl, COC1-20 alkyl, CONHC1-20 alkyl, C1-20 alkyl sulphonate, C1-20 alkyl phosphonate, C6-20 aryl, C4-20 heteroaryl, C1-4 alkyloxy C1-4 alkyl sulphonate, methyl (C1-4 alkyloxy C1-4 alkyl sulphonate)2, C1-4 alkyl terminally substituted with a C5-6 heterocyclyl with one or two heteroatoms being O, S or N, C _1-4 alkyl terminally substituted with N(C _1-4 alkyl)(C _1-4 alkyl), polyethylene glycol, an amino acid, zwitterionic (C1-4 alkyl)N ⁺ (C1-4 alkyl)2(C1-4 alkyl SO3-), (C1-4 alkyl)N ⁺ (C1-4 alkyl)2O-, cationic (C1-4 alkyl)N ⁺ (C _1-4 alkyl) ₃ , (C _1-4 alkyl)P ⁺ (C _1-4 alkyl) ₃ , (C _1-4 alkyl)P ⁺ (Ph) ₃ , and osamine; R ² , R ³ and R ⁴ are independently selected from the group consisting of hydrogen, halogen, NO ₂ , CN, CF ₃ , polyethylene glycol, C _1-20 alkyl, C _6-20 aryl, C _4-20 heteroaryl, C _1-20 alkyl sulphonate, and C _1-20 alkyl phosphonate; X and Y are independently selected from O or SO _m , where m=0-2; and A is selected from the group consisting of O, S, NR ⁵ , or Se, wherein R ⁵ is selected from the group consisting of H, C1-20 alkyl, COOH, COOC1-10 alkyl, COC1-20 alkyl, CONHC1-20 alkyl, C1-20 alkyl sulphonate, C _1-20 alkyl phosphonate, C _6-20 aryl, C _4-20 heteroaryl; for use in the treatment of skin conditions, such as acne, rosacea, psoriasis, vitiligo, skin conditions associated with systemic lupus erythematosus, Bowen’s disease, or actinic keratosis. In some embodiments R ¹ , R ² , R ³ , R ⁴ , R ⁵ , X, Y and A are as defined in any of the embodiments above. In another aspect, the invention relates to a compound of formula (I), for use in cancer diagnostics. In another aspect, the invention relates to a compound of formula (I), or a pharmaceutically acceptable salt thereof, wherein R ¹ is selected from a group consisting of C1-20 alkyl, C3-6 cycloalkyl, COOH, C1-20 COOH, COOC1-20 alkyl, COC _1-20 alkyl, CONHC _1-20 alkyl, C _1-20 alkyl sulphonate, C _1-20 alkyl phosphonate, C _6-20 aryl, C _4-20 heteroaryl, C1-4 alkyloxy C1-4 alkyl sulphonate, methyl (C1-4 alkyloxy C1-4 alkyl sulphonate)2, C1-4 alkyl terminally substituted with a C5-6 heterocyclyl with one or two heteroatoms being O, S or N, C1-4 alkyl terminally substituted with N(C1-4 alkyl)(C1-4 alkyl), polyethylene glycol, an amino acid, zwitterionic (C1-4 alkyl)N ⁺ (C1-4 alkyl)2(C1-4 alkyl SO3-), (C1-4 alkyl)N ⁺ (C1-4 alkyl)2O-, cationic (C1-4 alkyl)N ⁺ (C1-4 alkyl)3, (C1-4 alkyl)P ⁺ (C1-4 alkyl)3, (C1-4 alkyl)P ⁺ (Ph)3, and osamine; R ² , R ³ and R ⁴ are independently selected from the group consisting of hydrogen, halogen, NO2, CN, CF3, polyethylene glycol, C1-20 alkyl, C6-20 aryl, C4-20 heteroaryl, C1-20 alkyl sulphonate, and C1-20 alkyl phosphonate; X and Y are independently selected from O or SOm, where m=0-2; and A is selected from the group consisting of O, S, NR ⁵ , or Se, wherein R ⁵ is selected from the group consisting of H, C _1-20 alkyl, COOH, COOC _1-10 alkyl, COC _1-20 alkyl, CONHC _1-20 alkyl, C _1-20 alkyl sulphonate, C _1-20 alkyl phosphonate, C _6-20 aryl, C _4-20 heteroaryl; for use in the treatment or prevention of cancer. In some embodiments R ¹ , R ² , R ³ , R ⁴ , R ⁵ , X, Y and A are as defined in any of the embodiments above. In one embodiment, the treatment is photodynamic treatment of cancer. In one embodiment, the cancer is selected from the group consisting of skin cancer, basal cell skin cancer, squamous skin cancer, head and neck cancer, prostate cancer, lung cancer, gastrointestinal cancer, liver cancer, bile duct cancer, small intestine cancer, colon cancer, rectal cancer, prostate cancer, brain cancer, bladder cancer, and breast cancer. In one embodiment, the cancer is due to mutations in genes encoding specialized G4 helicases, such as FANCJ, PIF1 helicases, or DNA repair genes, such as BRCA1, BRCA2, TREX1, EXO1, CHEK2, ATM, Fanconi’s anemia genes, mismatch repair genes, PolB, APEX1, PALB2, TP53, and MRE11. In another aspect, the invention relates to a compound of formula (I), or a pharmaceutically acceptable salt thereof, wherein R ¹ is selected from a group consisting of C _1-20 alkyl, C _3-6 cycloalkyl, COOH, C _1-20 COOH, COOC _1-20 alkyl, COC _1-20 alkyl, CONHC _1-20 alkyl, C _1-20 alkyl sulphonate, C _1-20 alkyl phosphonate, C _6-20 aryl, C _4-20 heteroaryl, C1-4 alkyloxy C1-4 alkyl sulphonate, methyl (C1-4 alkyloxy C1-4 alkyl sulphonate)2, C1-4 alkyl terminally substituted with a C _5-6 heterocyclyl with one or two heteroatoms being O, S or N, C1-4 alkyl terminally substituted with N(C1-4 alkyl)(C1-4 alkyl), polyethylene glycol, an amino acid, zwitterionic (C1-4 alkyl)N ⁺ (C1-4 alkyl)2(C1-4 alkyl SO3-), (C1-4 alkyl)N ⁺ (C1-4 alkyl)2O-, cationic (C1-4 alkyl)N ⁺ (C1-4 alkyl)3, (C1-4 alkyl)P ⁺ (C1-4 alkyl)3, (C1-4 alkyl)P ⁺ (Ph)3, and osamine; R ² , R ³ and R ⁴ are independently selected from the group consisting of hydrogen, halogen, NO2, CN, CF3, polyethylene glycol, C1-20 alkyl, C6-20 aryl, C4-20 heteroaryl, C1-20 alkyl sulphonate, and C1-20 alkyl phosphonate; X and Y are independently selected from O or SOm, where m=0-2; and A is selected from the group consisting of O, S, NR ⁵ , or Se, wherein R ⁵ is selected from the group consisting of H, C1-20 alkyl, COOH, COOC1-10 alkyl, COC1-20 alkyl, CONHC1-20 alkyl, C1-20 alkyl sulphonate, C _1-20 alkyl phosphonate, C _6-20 aryl, C _4-20 heteroaryl; for use in treatment and prevention of ophthalmology conditions. In one embodiment, the ophthalmology condition is selected from the group consisting of age-related macular degeneration (AMD) (such as by stopping abnormal blood vessel growth below the macula), choroidal hemangioma, central serous chorioretinopathy (CSC), and polypoidal choroidal vasculopathy (PCV). In some embodiments R ¹ , R ² , R ³ , R ⁴ , R ⁵ , X, Y and A are as defined in any of the embodiments above. In another aspect, the invention relates to a compound of formula (I), or a pharmaceutically acceptable salt thereof, wherein R ¹ is selected from a group consisting of C1-20 alkyl, C3-6 cycloalkyl, COOH, C1-20 COOH, COOC1-20 alkyl, COC1-20 alkyl, CONHC1-20 alkyl, C1-20 alkyl sulphonate, C1-20 alkyl phosphonate, C6-20 aryl, C4-20 heteroaryl, C1-4 alkyloxy C1-4 alkyl sulphonate, methyl (C1-4 alkyloxy C1-4 alkyl sulphonate)2, C1-4 alkyl terminally substituted with a C5-6 heterocyclyl with one or two heteroatoms being O, S or N, C _1-4 alkyl terminally substituted with N(C _1-4 alkyl)(C _1-4 alkyl), polyethylene glycol, an amino acid, zwitterionic (C _1-4 alkyl)N ⁺ (C _1-4 alkyl) ₂ (C _1-4 alkyl SO ₃ -), (C _1-4 alkyl)N ⁺ (C _1-4 alkyl) ₂ O-, cationic (C _1-4 alkyl)N ⁺ (C _1-4 alkyl) ₃ , (C _1-4 alkyl)P ⁺ (C _1-4 alkyl) ₃ , (C _1-4 alkyl)P ⁺ (Ph) ₃ , and osamine; R ² , R ³ and R ⁴ are independently selected from the group consisting of hydrogen, halogen, NO ₂ , CN, CF ₃ , polyethylene glycol, C _1-20 alkyl, C _6-20 aryl, C _4-20 heteroaryl, C _1-20 alkyl sulphonate, and C _1-20 alkyl phosphonate; X and Y are independently selected from O or SOm, where m=0-2; and A is selected from the group consisting of O, S, NR ⁵ , or Se, wherein R ⁵ is selected from the group consisting of H, C1-20 alkyl, COOH, COOC1-10 alkyl, COC1-20 alkyl, CONHC1-20 alkyl, C1-20 alkyl sulphonate, C1-20 alkyl phosphonate, C6-20 aryl, C4-20 heteroaryl; for use in photodynamic therapy for treatment of infections caused by bacteria, viruses, yeast, or fungi. Examples of such infections are infections caused by herpes and papilloma viruses, infections associated with brain abscesses and non-healing ulcers, dental infections including periodontitis and endodontics, as well as cutaneous Leishmaniasis. In some embodiments R ¹ , R ² , R ³ , R ⁴ , R ⁵ , X, Y and A are as defined in any of the embodiments above. In another aspect, the invention relates to a method for preparing a 1H- benzo[7,8]thioxantheno[2,1,9-def]isoquinoline-1,3(2H)-dione according to present invention comprising the steps of: a. subjecting an aromatic thiazole to basic reflux conditions; b. subjecting the resulting compound to a 4-bromo-1,8-naphthylic anhydride; and subjecting the resulting compound to an amino derivative at elevated temperature. All aspects and embodiments disclosed herein can be combined with any other aspect and/or embodiment disclosed herein. The invention is further illustrated by means of the following examples, which do not limit the invention in any respect, and in which standard techniques known to the skilled chemist and techniques analogous to those described in these examples may be used where appropriate. All cited documents and references mentioned herein are incorporated by reference in their entireties. EXAMPLES Preparation of compounds General methods Reagents and chemicals from commercial sources were used without further purification. Edinburgh minimal media was prepared (EMM2) according to Cold Spring Harb Protoc 2016 standard recipe. Solvents were dried and purified using standard techniques, readily understood by one skilled in the art. Silica gel chromatographies were performed on technical grade silica gel, with a pore size of 60 Å and a 230-400 mesh particle size, packed with analytical-grade solvents. NMR spectra were recorded with a Bruker AVANCE III 300 ( ¹ H, 300 MHz and ¹³ C, 75MHz) spectrometer unless stated otherwise. Chemical shifts are given in ppm relative to TMS and coupling constants J in Hz. UV-vis spectra were recorded on a Shimadzu UV-1800 spectrometer. High-resolution mass spectrometry (HRMS) was performed with a JEOL JMS-700 B/E. Preparation of starting materials The starting materials for the Examples above are either commercially available or are readily prepared by the standard methods from known materials. For example, the following reactions are an illustration, but not a limitation, of some of the starting materials used in the above reactions. Method 1 6-(naphthalen-1-yl)-7-nitro-2-(pentan-3-yl)-1H-benzo[de]isoq uinoline-1,3(2H)-dione A mixture of N-(2-ethylhexyl)-4-bromo-5-nitro-1,8-naphtylimide (300 mg, 0.77 mmol), 1- naphtylboronic acid (198 mg, 1.15 mmol), tetrakis(triphenylphosphine)palladium (44 mg , 0.038 mmol, 289 mg) and potassium carbonate (317 mg, 2.30 mmol), water (0.76 mL), and dioxane (3.1 mL) was refluxed under argon atmosphere and monitored by TLC. The mixture was cooled to room temperature and extracted with CH2Cl2 / water. After drying over MgSO4, the solvent was removed by rotary evaporation and the crude material was subjected to silica gel column chromatography using petroleum ether/CH2Cl2 as eluent. A red powder was obtained (300 mg, 89%). ¹ H NMR (300 MHz, CDCl3) δ 8.78 (d, J = 7.6 Hz, 1H), 8.68 (d, J = 7.8 Hz, 1H), 8.01 – 7.90 (m, 3H), 7.84 (d, J = 7.8 Hz, 1H), 7.64 (d, J = 8.4 Hz, 1H), 7.59 – 7.51 (m, 1H), 7.50 – 7.40 (m, 2H), 7.27 – 7.20 (m, 1H), 5.15 – 4.99 (m, 1H), 2.35 – 2.20 (m, 2H), 2.06 – 1.86 (m, 2H), 0.95 (t, J = 7.5 Hz, 6H). Method 2 6-((1-nitronaphthalen-2-yl)oxy)-1H,3H-benzo[de]isochromene-1 ,3-dione DMF (100 mL) was added to a solid mixture of 6-bromo-1H, 3H-benzo[de]isochromene-1,3- dione (1 g, 3.61 mmol), 1-nitronaphthalen-2-ol (751 mg, 3.97 mmol), and potassium carbonate (274 mg, 1,99 mmol). The mixture was refluxed for 4 h, after which it was cooled down, and a mixture of water (200 mL) and concentrated HCl (0.5 mL) was added. The obtained solid was filtered and washed with water and methanol to afford the title compound (881 mg, 63%). ¹ H NMR (300 MHz, DMSO-d6) δ 8.79 (dd, J = 8.5, 1.2 Hz, 1H), 8.67 (dd, J = 7.3, 1.1 Hz, 1H), 8.47 (t, J = 8.5 Hz, 2H), 8.30 – 8.24 (m, 1H), 8.04 (dd, J = 8.5, 7.3 Hz, 1H), 7.94 – 7.84 (m, 2H), 7.81 (ddd, J = 8.1, 6.2, 2.1 Hz, 1H), 7.74 (d, J = 9.1 Hz, 1H), 7.25 (d, J = 8.3 Hz, 1H). Method 3 6-((1-aminonaphthalen-2-yl)oxy)-1H,3H-benzo[de]isochromene-1 ,3-dione Glacial acetic acid (20 mL) was added to a solid mixture of 6-((1-nitronaphthalen-2-yl)oxy)- 1H,3H-benzo[de]isochromene-1,3-dione (500 mg, 1.30 mmol) and iron powder (507 mg, 9.08 mmol). The mixture was refluxed for 1 h. The mixture was then cooled down and water was added. The obtained solid was filtered off and purified by silica-gel column chromatography (CH ₂ Cl ₂ /EtOAc, 60/40) to afford the title compound (402 mg, 87%) NMR (300 MHz, DMSO- d ₆ ) δ 8.97 (dd, J = 8.4, 1.2 Hz, 1H), 8.63 (dd, J = 7.3, 1.2 Hz, 1H), 8.41 (d, J = 8.4 Hz, 1H), 8.30 – 8.21 (m, 1H), 7.99 (dd, J = 8.4, 7.3 Hz, 1H), 7.90 – 7.83 (m, 1H), 7.54 – 7.44 (m, 2H), 7.25 (d, J = 2.3 Hz, 2H), 6.82 (d, J = 8.4 Hz, 1H), 5.82 (s, 2H). Method 4 1H,3H-benzo[a]isochromeno[4,5,6-jkl]xanthene-1,3-dione DMF (6 mL) was added to 6-((1-aminonaphthalen-2-yl)oxy)-1H, 3H-benzo[de]isochromene-1,3- dione (300 mg, 844.24 mmol). Isopentyl nitrite (0,34 mL, 2.53 mmol) was added dropwise, and the solution was refluxed for 1 h. The solvent was removed under reduced pressure, and the crude product was purified by silica-gel column chromatography (CH2Cl2/EtOAc, 80/20) to afford the title compound (57 mg, 20%). EXAMPLE 1 2-(pentan-3-yl)-1H-benzo[7,8]thioxantheno[2,1,9-def]isoquino line-1,3(2H)-dione (DBI) A solution of 2-methylnaphtho[1,2-d]thiazole (10 g, 50.2 mmol) in a mixture of ethylene glycol and aqueous 50% NaOH (v/v = 5/1, 120 mL) was refluxed under argon for 16 h before being poured into an ice-water bath and acidified to pH = 3 with 1M HCl solution. The organic phase was then extracted with CH ₂ Cl ₂ , dried over MgSO ₄ , and concentrated under reduced pressure. The resulting crude 1-aminonaphthalene-2-thiol was directly engaged in the next step without further purification. The crude mixture was blended with 4-bromo-1,8-naphthalic anhydride (11.0 g, 39.7 mmol) and potassium carbonate (5.49 g, 39.7 mmol). DMF (270 mL) was then added under air atmosphere and the reaction mixture was stirred for 16 h at room temperature. Isopentyl nitrite (15.7 mL, 119.1 mmol) was then added. An orange precipitate appeared upon stirring at 60 °C. After 24 h, the latter was filtrated, successively washed with water and methanol, and finally dried with a rotary evaporator under reduced pressure. The resulting powder was directly added to a flask containing 3-aminopentane (5.33 mL, 45.7 mmol) and imidazole (77 g). This mixture was stirred for 16 h at 100 °C before being cooled down to room temperature. Then, a 1 M aqueous solution of HCl was gently added and the aqueous phase was subsequently extracted with CH ₂ Cl ₂ , dried over MgSO ₄ , and concentrated under reduced pressure. The crude was purified by column chromatography on silica gel (eluent: CH ₂ Cl ₂ ) affording an orange solid NMR (300 MHz, CDCl ₃ ): δ (ppm) 8.72 – 8.58 (m, 2H), 8.45 – 8.38 (m, 2H), 7.90 – 7.83 (m, 1H), 7.80 (d, J = 8.6 Hz, 1H), 7.59 – 7.50 (m, 3H), 7.39 (d, J = 8.6 Hz, 1H), 5.15 – 5.02 (m, 1H), 2.36 – 2.20 (m, 2H), 2.00 – 1.84 (m, 2H), 0.91 (t, J = 7.5 Hz, 6H). ¹³ C NMR (75 MHz, CDCl ₃ ): δ (ppm) 139.1, 136.8, 134.0, 133.5, 131.6, 130.4, 130.4, 129.2, 129.1, 127.5, 126.7, 125.9, 125.7, 124.0, 123.1, 121.1, 120.0, 118.6, 57.5, 25.1, 11.5. HRMS (MALDI): m/z calcd for C ₂₇ H ₂₁ NO ₂ S: 423.1288, found: 423.1293. Monocrystals were obtained by slow evaporation of chloroform. EXAMPLE 2 2-(pentan-3-yl)benzo[lmn]naphtho[2,1-c][2,8]phenanthroline-1 ,3(2H,6H)-dione A solution of 6-(naphthalen-1-yl)-7-nitro-2-(pentan-3-yl)-1H-benzo[de]isoq uinoline-1,3(2H)- dione (250 mg, 0.57 mmol) and triphenylphosphine (449 mg, 1.71 mmol) in 7 ml of 1,2- dichlorobenzene was refluxed under argon. The mixture was cooled to room temperature and was then subjected directly to silica gel column chromatography using chloroform as eluent. The title compound was obtained as a red powder (200 mg, 86%). ¹ H NMR (500 MHz, DMSO-d6) δ 12.28 (s, 1H), 8.99 (d, J = 8.6 Hz, 1H), 8.50 – 8.36 (m, 2H), 8.31 (d, J = 8.8 Hz, 1H), 8.08 (d, J = 8.8 Hz, 1H), 8.02 (dd, J = 8.0, 1.5 Hz, 1H), 7.75 – 7.67 (m, 1H), 7.57 (ddd, J = 7.9, 6.9, 1.0 Hz, 1H), 7.51 (d, J = 8.8 Hz, 1H), 5.03 (tt, J = 10.2, 5.6 Hz, 1H), 2.27 – 2.15 (m, 2H), 1.87 – 1.76 (m, 2H), 0.78 (t, J = 7.5 Hz, 6H). ¹³ C NMR (126 MHz, DMSO-d6) δ 142.9, 138.4, 137.7, 133.2, 131.2, 130.6, 129.9, 129.4, 128.8, 128.1, 125.3, 123.2, 122.2, 117.4, 116.9, 112.3, 105.7, 55.6, 24.3, 11.4. HRMS (MALDI-TOF) m/z calcd for C23H22N3O4: 406.1675, found 406.1676. EXAMPLE 3 2-(pentan-3-yl)-1H-benzo[7,8]xantheno[2,1,9-def]isoquinoline -1,3(2H)-dione 1H, 3H-benzo[a]isochromeno[4,5,6-jkl]xanthene-1,3-dione (40 mg, 0.12 mmol) was dissolved in DMF (1 mL).3-aminopentane (15 ^L, 0.13 mmol) was added and the mixture was subjected to 120 °C overnight. The mixture was then concentrated under reduced pressure and the obtained solid was purified by silica-gel column chromatography (CH ₂ Cl ₂ ) to afford the title compound (36 mg, 75%). ¹ H NMR (300 MHz, CDCl3) δ 8.84 (d, J = 8.6, 1.0 Hz, 1H), 8.59 (d, J = 8.1 Hz, 1H), 8.54 (d, J = 8.3 Hz, 1H), 8.41 (d, J = 8.1, 0.7 Hz, 1H), 7.92 – 7.85 (m, 2H), 7.66 (ddd, J = 8.6, 6.9, 1.5 Hz, 1H), 7.54 (ddd, J = 8.0, 6.9, 1.1 Hz, 1H), 7.39 (d, J = 8.9 Hz, 1H), 7.24 (d, J = 8.4 Hz, 1H), 5.10 (q, J = 9.5, 5.9 Hz, 1H), 2.37 – 2.20 (m, 2H), 1.94 (m, J = 14.9, 7.5, 5.9 Hz, 2H), 0.93 (t, J = 7.5 Hz, 6H). ¹³ C NMR (76 MHz, CDCl ₃ ) δ 155.13, 152.41, 133.75, 133.23, 131.71, 130.25, 129.47, 128.26, 125.82, 124.05, 120.66, 119.18, 117.65, 113.51, 109.31, 57.26, 25.01, 11.38. HRMS (FAB): m/z calcd for C27H21NO3: 407.1521, found: 407.1523. EXAMPLE 4 3-(1,3-dioxo-1H-benzo[7,8]thioxantheno[2,1,9-def]isoquinolin -2(3H)-yl)-N,N,N- trimethylpropan-1-aminium To a solution 2-(3-(dimethylamino)propyl)-1H-benzo[7,8]thioxantheno[2,1,9- def]isoquinoline- 1,3(2H)-dione (50 mg, 0.118 mmol) in DMF (3 mL) was added dropwise iodomethane (26 µL, 0.41 mmol). The reaction mixture was stirred at 60 °C overnight. The solvent and iodomethane were then removed by rotary evaporation. The title compound was obtained as an orange reddish powder (65 mg, 99%). ¹ H NMR (300 MHz, DMSO-d6) δ 8.62 – 8.50 (m, 1H), 8.45 (d, J = 8.1 Hz, 1H), 8.34 (d, J = 8.1 Hz, 1H), 8.22 (d, J = 8.0 Hz, 1H), 8.03 – 7.92 (m, 2H), 7.68 (d, J = 7.9 Hz, 1H), 7.62 – 7.55 (m, 2H), 7.52 (d, J = 8.0 Hz, 1H), 4.12 (t, J = 6.3 Hz, 2H), 3.48 – 3.37 (m, 3H), 3.04 (s, 9H), 2.14 (p, J = 8.6, 7.2 Hz, 2H). ¹³ C NMR (76 MHz, DMSO-d ₆ ) δ 163.2, 162.6, 138.4, 135.8, 133.5, 132.8, 131.3, 130.8, 130.6, 130.3, 129.3, 129.1, 128.1, 127.9, 126.7, 125.8, 124.3, 123.5, 123.1, 120.3, 119.9, 117.5, 63.3, 52.2, 52.1, 36.8, 21.6. HRMS (MALDI-TOF) calcd for C ₂₈ H ₂₅ N ₂ O ₂ S: 453.1631, found 453.1635. EXAMPLE 5 3-(1,3-dioxo-1H-benzo[7,8]thioxantheno[2,1,9-def]isoquinolin -2(3H)-yl)-N,N-dimethylpropan- 1-amine oxide To a solution 2-(3-(dimethylamino)propyl)-1H-benzo[7,8]thioxantheno[2,1,9- def]isoquinoline- 1,3(2H)-dione (50 mg, 0.118 mmol) in ethanol (13 mL) was added dropwise commercial H2O2 (30%, 128 µL, 1.26 mmol). The reaction mixture was stirred at reflux temperature overnight. The solvent and H ₂ O ₂ were then removed by rotary evaporation. The title compound was obtained as an orange reddish powder (51 mg, 99%). ¹ H NMR (300 MHz, CDCl ₃ ) δ 8.66 – 8.47 (m, 2H), 8.32 (dd, J = 8.0, 2.7 Hz, 1H), 7.90 – 7.75 (m, 1H), 7.71 (d, J = 8.5 Hz, 1H), 7.51 – 7.40 (m, 3H), 7.27 (d, J = 8.6 Hz, 1H), 4.28 (t, J = 6.7 Hz, 2H), 3.48 (t, J = 8.2 Hz, 2H), 3.24 (s, 3H), 2.39 – 2.30 (m, 2H). HRMS (MALDI-TOF) calcd for C27H23N2O3S: 455.1421, found 455.1421. EXAMPLE 6 3-(1,3-dioxo-1H-benzo[7,8]thioxantheno[2,1,9-def]isoquinolin -2(3H)-yl)propanoic acid To a mixture of 1H,3H-benzo[7,8]thioxantheno[2,1,9-def]isochromene-1,3-dione (200 mg, 0.56 mmol) and β-alanine (100 mg, 1.13 mmol) was added DMF (4 mL ). The reaction mixture was stirred at reflux temperature for 24 h before being extracted with EtOAc, water and brine. After drying over MgSO4, the solvent was removed by rotary evaporation and the crude material was subjected to silica gel column chromatography using CHCl3 as eluent. The title compound was obtained as an orange powder (195 mg, 81%). ¹ H NMR (300 MHz, DMSO-d ₆ ) δ 8.43 (d, J = 8.4 Hz, 1H), 8.28 (d, J = 8.0 Hz, 1H), 8.15 (d, J = 8.1 Hz, 1H), 8.05 (d, J = 7.8 Hz, 1H), 7.87 (dd, J = 17.6, 8.2 Hz, 2H), 7.56 – 7.44 (m, 3H), 7.37 (d, J = 8.5 Hz, 1H), 4.19 (t, J = 7.8 Hz, 2H), 2.57 (t, J = 7.8 Hz, 2H). ¹³ C NMR (76 MHz, DMSO- d ₆ ) δ 172.5, 162.7, 162.0, 138.2, 135.6, 133.4, 132.7, 131.1, 130.6, 130.4, 130.0, 129.0, 127.8, 127.6, 126.6, 125.6, 124.1, 123.5, 122.9, 120.0, 119.7, 117.2, 35.7, 32.1. HRMS (MALDI-TOF) calcd for C ₂₅ H ₁₅ NO ₄ S: 425.0716, found 425.0723. EXAMPLE 7 2-(3-(dimethylamino)propyl)-1H-benzo[7,8]thioxantheno[2,1,9- def]isoquinoline-1,3(2H)-dione To a solution of 1H,3H-benzo[7,8]thioxantheno[2,1,9-def]isochromene-1,3-dione (500 mg, 1.41 mmol) in ethanol (10 mL) was added dropwise N ¹ ,N ¹ -dimethylpropane-1,3-diamine (355 µL, 2.82 mmol). The reaction mixture was stirred at reflux temperature for 36 h before being extracted with CH ₂ Cl ₂ , water and brine. After drying over MgSO ₄ , the solvent was removed by rotary evaporation and the crude material was subjected to silica gel column chromatography using CHCl3 as eluent. The title compound was obtained as an orange powder (150 mg, NMR (300 MHz, CDCl3) δ 8.69 – 8.52 (m, 2H), 8.39 (t, J = 8.0 Hz, 2H), 7.91 – 7.81 (m, 1H), 7.78 (d, J = 8.6 Hz, 1H), 7.56 – 7.45 (m, 3H), 7.35 (d, J = 8.6 Hz, 1H), 4.25 (t, J = 7.6 Hz, 2H), 2.45 (t, J = 7.4 Hz, 2H), 2.27 (s, 3H), 1.93 (p, J = 7.4 Hz, 2H). HRMS (MALDI-TOF) calculated for C27H23N2O2S: 439.1475, found 439.1480. BIOLOGICAL ASSAYS Cellular oxidative stress (figure 1) The ability of DBI to generate cellular oxidative stress was evaluated. CellROX™ green reagent was used as a fluorogenic probe for detecting oxidative stress in the nucleus of live cells. This dye is weakly fluorescent in a reduced state while displaying bright green fluorescence upon oxidation by ROS. Human cervical epithelioid carcinoma (HeLa) cells treated with DBI (1 µM) and irradiated with blue light showed a bright green fluorescent signal mainly localized in the cell nucleus supporting the ability of DBI to generate ROS. Importantly, control experiments performed in the absence of both DBI and light as well as in the presence of either DBI or light showed negligible ROS-associated nuclear fluorescent signal, indicating that intracellular ROS production only occurs in light irradiated DBI-treated cells, thereby confirming its potential usefulness for the targeted applications. Quantification of the nuclear ROS signal in non-irradiated and irradiated DBI-treated HeLa cells are shown in figure 1. The data represent populations of individual cells (N = 50 cells) and Means ± SD are indicated. Analysis of the data was performed using two-sample t test and p value is indicated. Phototherapeutic efficacy toward HeLa and breast cancer cell lines (figures 2 - 4) The phototherapeutic efficacy of the compounds prepared in Examples 1, 2 and 3 here above toward HeLa and breast (MCF-7) cancer cell lines was determined using the PrestoBlue™ cell viability assay (Invitrogen). Briefly, 5000 HeLa cells/well and 4000 MCF-7 cells/well were seeded in complete culture medium (Dulbecco´s modified eagle medium (DMEM) supplemented with penicillin-streptomycin (1×), and 10% fetal bovine serum) on 96-well plates the day before the treatment. Compounds were dissolved in the culture medium at the indicated concentrations and added to the cells. At 48 h after treatment, 10 μL of PrestoBlue was added to each well and the cells were incubated at 37 °C for three additional hours. HeLa and MCF-7 cells were then treated with various concentrations the compounds prepared in Example 1, 2 and 3 (ranging from 0 to 0.3 µM) for 24 h, followed by irradiation for 8 minutes with blue light (18 mW cm ^-2 ) using a LED light cube (470/22 nm), and further incubated for 24 h. These experimental conditions were optimized in order to avoid cell death caused by overexposure to light and to match the incubation time and general experimental conditions used in the dark cytotoxicity studies. In the absence of light irradiation, no cytotoxicity was observed for either HeLa or MCF-7 cells treated with various concentrations of the compounds prepared in Example 1, 2 and 3 (ranging from 0 to 25 µM) even after 48 h of continued drug exposure. Cell viability was measured by recording the fluorescence signal of PrestoBlue (λexc/λem: 560/590 nm) using a Synergy H4 microplate reader (Biotek). The results show that the compounds of the present invention exhibit very high photocytotoxic activity. The results are shown in table 1 below, and in figures 2-4. Figure 2a shows the effect of Example 1 (DBI) on HeLa cells and figure 2b shows the effect of DBI on MCF-7 cells. Figure 3a shows the effect of the compound of Example 2 with no light and figure 3b shows the effect of the compound of Example 2 with light. Figure 4a shows the effect the compound of Example 3 with no light and figure 4b shows the effect the compound of Example 3 with light. Table 1. IC50 values and high dark IC50/light IC50 phototoxic index (PI) ratios LIVE/DEAD™ assay used to determine the viability of HeLa cells. The compound of Example 1 (DBI) photo-triggered cancer cell death was also confirmed by using a LIVE/DEAD™ viability/cytotoxicity stain assay. HeLa cells were treated with DBI (1 µM) or with an equivalent amount of DMSO (0.02 % v/v) and incubated at 37 °C for 24 h. Blue light (18 mW cm ^-2 ) was applied in the same manner as in the “Phototherapeutic efficacy toward HeLa and breast cancer cell lines” experiment and the cells were further incubated at 37 °C for additional 24 h. LIVE/DEAD™ fixable red stain for cytotoxicity detection (1 µL /mL) was added to the cells for 30 min at 37 °C before PFA fixation. λexc/λem: 598/630-730 nm. Only the DBI-treated HeLa cells subjected to light irradiation displayed a bright red signal indicative of cell death due to ruptured plasma membrane. Phototherapeutic efficiency toward multicellular tumor organoids (Figure 5) The hypoxic microenvironment of solid tumors is characterized by a severe O ₂ shortage that can hamper therapeutic outcomes in highly O ₂ -dependent PSs (Singleton, D.C., et al. Nat Rev Clin Oncol 18, 751-772 (2021)). Remarkably, DBI showed high phototoxicity towards murine pancreatic tumor 3D organoids with IC50 = 16.1 ± 7.5 nM that matched the IC50 values obtained from the 2D monolayer human cell cultures. These results confirm the high phototherapeutic efficacy of DBI even in systems with reduced oxygen supply. These results are shown in figure 5. Yeast cell oxidative stress The effect of DBI on the growth of yeast cells was investigated. Solutions of Schizosacharomyces pombe yeast cells in EMM2 liquid media containing either DMSO, or 1, 2, 5, or 10 nM of DBI were prepared. After 30 min, the solutions were treated with 20% blue light intensity for 20 min. After light treatment, the yeast cultures were left overnight to allow the yeast cells to grow. The total amount of cells in each solution was then counted. The results are shown in figure 6. The growth of yeast cells was clearly affected by the presence of DBI in combination with light treatment already at DBI concentrations of 2 nM. However, the presence of DBI without light treatment did not reduce the growth at all. Photo-induced DNA damage and G-quadruplex formation The ability of DBI to increase the intracellular 8-oxoG distribution in a light-dependent manner was investigated. Photo-irradiated DBI-treated HeLa cells showed a significant enrichment in 8- oxoG formation ~3.1-fold compared to mock-treated cells (p = 9.3×10 ^-19 ), indicating enhanced levels of oxidative damage to the genome. Thereafter, it was determined whether elevated 8-oxoG formation results in double stranded breaks, (DSBs). The anti-γH2AX antibody, an established marker of DSBs, was used to assess the induction of DNA damage. A ~11.3-fold higher DSB levels in photo-irradiated DBI-treated cells was observed compared to the control cells (p = 1.5×10 ^-32 ), demonstrating that DBI induces a substantial amount of damage into the genome as a very promising candidate for photodynamic cancer therapy. The interplay among guanine oxidation, DSBs and G4 formation was then determined. The G4- specific antibody BG4 was used to detect about 2.6-fold higher levels of nuclear BG4 foci in DBI- treated HeLa cells subjected to light irradiation, compared to the controls (p = 6.6×10 ^-26 ), demonstrating G4 formation induction. As G4s are known obstacles to DNA replication progression and can stall DNA polymerases and thereby induce DNA damage in the form of single strand breaks (SSBs) or DSBs, the increased levels of G4 structures in the genome may also be interpreted as a trigger for DSBs, if the levels of G4s are too high for specialized G4 helicases to resolve these structures in a timely manner. These data show that DBI- photogenerated ROS can result in mutagenic events in which, the oxidation of guanine bases in G-rich genomic regions can induce DNA-damage activation and induce G4 formation. In vivo validation of DBI photo-induced cytotoxic effect in zebrafish embryos. Zebrafish are relevant models for human drug discovery not only because of the conserved physiology between humans and zebrafish, but also because about 70% of human protein coding genes have a zebrafish gene orthologue, and that the drug metabolism pathways are conserved. Zebrafish embryos are also translucent and allow real-time monitoring of drug uptake. Because DBI is emissive, its accumulation in zebrafish was monitored. Wildtype zebrafish embryos were dechorionated at the 6-somite stage, twelve hours post fertilization (hpf), and treated with DBI in the embryo medium for twelve hours in dark, until they reached the prim-5 stage (24 hpf). The DBI-treated 24 hpf embryos showed a widespread fluorescence signal along the whole embryonic body confirming effective uptake of the drug. The photocytotoxic effect of DBI on the embryos treated with different concentrations of DBI after light irradiation was investigated. Already after 15 min post light treatment, morphological changes were detected in the embryos, particularly in the tails, with an increasing severity correlated to increased DBI concentration. Importantly, these morphological changes were not detected in the no light-treated embryos even at the highest DBI concentration treatment. These data demonstrate an efficient phototoxicity of DBI in vivo, suggesting a similar light-induced effect of DBI in an intact animal as found in our cell culture- based experiments. Immunofluorescence experiments with the BG4 and 8-oxoG antibodies, and TUNEL assays were performed to detect apoptotic DNA fragmentation. DBI-treated embryos subjected to light exposure clearly showed an increased level of fluorescence signals associated to TUNEL, BG4, and 8-oxoG compared to mock-treated embryos, again highlighting the ability of DBI to induce cytotoxic effects in an exclusively light-dependent manner. Damage sites and dying cells were detected throughout the whole embryos, with an emphasis on the tails and the most superficial tissue layers. This last finding may be correlated with the high proliferative activity of the tails of the embryos at this particular growing stage. A similar set of experiments performed with older embryos showed a marked DBI-associated fluorescence signal in the tails with almost no accumulation in other compartments. These photo-irradiated DBI-treated embryos showed DNA damage primarily confined in the tails indicating that the photo-driven toxic effects exerted by DBI could be restricted only to the compound-targeted area. Importantly, embryos treated with DBI in the dark (no light exposure) did not show neither significant morphological alterations nor did they provide any indication of DNA damage. Together, these data show that DBI is a PS with minimal side-effects into untreated areas and highlight the benefits of DBI in PDT. Subcellular localization of DBI in ILVs Live-cells imaging Fluorescence of DBI was detected as bright foci inside the cytoplasm and absent within the nucleus of live cells the details of cytoplasmic localization. HeLa cells were treated with DBI (500 nM) and incubated for 20 min. HeLa cells were co-stained with the nuclear dye Hoechst 33342 (500 nM, blue signal). λexc/λem: 405/420-460 nm for Hoechst (blue signal); and 528/540-750 nm for DBI (green signal).2D single plane images were constructed by maximum intensity projection, where the highest intensity of each plane of Z-stacked images were used. The DBI signal that overlap with Hoechst are not within the nucleus. Immunofluorescence experiments To determine the exact sub-localization of DBI, immunofluorescence experiments were performed using a set of organelle-specific antibodies. Anti-LAMP1, anti-EEA1 and anti-CD63 antibodies were used as lysosome, early endosome, and ILV markers, respectively. HeLa cells were treated with DBI (1 µM) for 24 h and either non- irradiated or irradiated with a blue LED light cube (20 mW cm ^-2 ) for 20 min and incubated for additional 30 min at 37 °C before paraformaldehyde (PFA) fixation. λ _exc /λ _em : 405/440-460 nm for Hoechst (blue signal); and 528/540-590 nm for DBI (green signal); and λ _exc /λ _em : 598/620-750 nm for anti-LAMP1, anti-EEA1 and anti-CD63 (red signal). Anti-LAMP1, anti-EEA1 and anti-CD63 antibodies were used as lysosome, early endosome, and ILV markers, respectively. Without light irradiation, no apparent co-localization between DBI and anti-LAMP1 or anti-EEA1 antibodies could be detected, excluding its accumulation in lysosomes and early endosomes. Conversely, DBI signal perfectly matched the anti-CD63 signal, suggesting that DBI localizes in the ILVs. Intracellular distribution of DBI after light exposure Under light-activated conditions, the signals of anti-CD63 and DBI remained overlapped. In both non-irradiated and even more in irradiated cells treated with DBI it was observed that the signal of the PS co-localized with the signal of Hoechst in the ILVs. Hoechst is a nuclear dye that preferentially binds double-stranded DNA (dsDNA). These findings suggest the ability of DBI to target DNA molecules inside the ILVs. To determine if DBI and Hoechst were bound on the surface or inside the ILVs, cells were treated with deoxyribonuclease (DNase), which has been shown to degrade the DNA inside the nucleus and only the DNA that is attached to the outer membrane of the vesicles (Thakur, B.K. et al. Cell Res 24, 766-9 (2014) and Yokoi, A. et al. Sci Adv 5, eaax8849 (2019)). In DNase I- treated cells, the fluorescence signal from the nucleus disappeared, indicating that the DNase I- treatment was successful. However, the cytoplasmic signal from Hoechst and the DBI signal were unaffected, demonstrating that both DBI and Hoechst localized inside the ILVs. In addition, in light-treated cells, the fluorescent signal of Hoechst was enhanced compared to non- irradiated conditions, suggesting an increased level of DNA in the ILVs supporting the theory that the use of genotoxic drugs increases DNA abundance in exosomes. The data provide solid evidence of the uptake of DBI inside the ILVs, and show that DBI causes DSBs and genomic instability through a light-induced oxidative stress which results in increased amounts of DNA inside the ILVs or exosomes when released outside the cells.